My question: If macroevolution is true, why hasnÃ¢â‚¬â„¢t malaria won the war against humans-why arenÃ¢â‚¬â„¢t we all dead? Malaria has a tremendous advantage in the mutation race: there are ~1 trillion malaria parasites in just one person. If malaria could fundamentally change (macro evolution with multiple positive mutations) then it should have overcome sickle cell (malaria in its large numbers has never overcome sickle cell), be more adaptive to temperature (move outside the 10/40 window) and create a strain that is unbeatable by man. My guess is that there been more malaria parasites in the last 50 years than all the mammals put together in the last 100 million years. With the shear numbers of malaria, why have they not seen macro evolution?

I was summarized a good point BeheÃ¢â‚¬â„¢s was making in his book Ã¢â‚¬Å“The Edge of EvolutionÃ¢â‚¬Â. This was written in debate on another blog in response to a question on how parasites mutates to adapt to antibiotics/insecticides. This is what made me think of that question above.

The effects of mutations are best studied where we have extremely large sample sizes. The three best largest sample sizes that have studied mutations are:

1) Malaria- a person sick with malaria can have up to a trillion parasites and there are ~ 500 million people who get sick with this malaria every year. Because of the shear numbers this is a good candidate to study what random mutation can and can not do.2) HIV- The mutation rate for people with HIV can be up to 10,000 times faster than an unaffected person.3) E-coli- Dr. Richard Lenski at Michigan State has studied e-coli for many years and has used a large sample size: Not near as big as either HIV or malaria but significant.

In the malaria case, they have found that breaking things is far easier than making systems. In other words a destructive mutation can be beneficial. The best example is sickle cell. In America it has been an unmitigated disaster while in Africa it is beneficial in the fight with malaria. This is equivalent to using your hand to stopping swords killing blow- you survive but your hand is a bloody mess.

In most of these cases it was just one beneficial mutation, usually just an amino acid switch: An exception is C Harlem (2 amino acid switches). Important observations from these huge numbers are:

1. We are able to quantify positive mutation numbers with these large samples. Remember that a positive mutation is usually a negative mutation with a positive result (sickle cell, HbS, ThalassemiaÃ¢â‚¬Â¦) Scientist use these numbers when developing antibiotics. For example, if there is a 1/100 million chance of adaptation and there are 1 trillion malaria parasites in the person then scientist knows they have to make cocktail (2 or more) antibiotics to overcome malaria adaptations.

2. With these large numbers we have only seen 1 and rarely 2 positive mutations for any adaptation. Each additional mutation is like adding an additional power ball to the lotto: i.e. the odds get significantly worse with each addition ball/mutation. The odds of just one mutation in is ~10^12 and for 2 it is 10^20 with malaria. As far as I know we have never seen 3 positive mutations- which is good IMO. Why, because Malaria has a tremendous advantage in the mutation race: there are 1 trillion malaria parasites in just one person. If malaria could fundamentally change (macro evolution with multiple positive mutations) then it should have overcome sickle cell (malaria in its large numbers has never overcome sickle cell), be more adaptive to temperature (move outside the 10/40 window) and create a strain that is unbeatable by man. In other words, evolution strongly favors malaria.3. Life has systems that would require thousands of positive mutations if not millions of positive mutations. Things like a caterpillar metamorphosing into a butterfly where every transitional step is lethal and consequently the process would require millions of positive mutations without failure: Statistically this is impossible. In other words, our evolution theory needs to evolve.

My question: If macroevolution is true, why hasnÃ¢â‚¬â„¢t malaria won the war against humans-why arenÃ¢â‚¬â„¢t we all dead? Malaria has a tremendous advantage in the mutation race: there are ~1 trillion malaria parasites in just one person. If malaria could fundamentally change (macro evolution with multiple positive mutations) then it should have overcome sickle cell (malaria in its large numbers has never overcome sickle cell), be more adaptive to temperature (move outside the 10/40 window) and create a strain that is unbeatable by man. My guess is that there been more malaria parasites in the last 50 years than all the mammals put together in the last 100 million years. With the shear numbers of malaria, why have they not seen macro evolution?I was summarized a good point BeheÃ¢â‚¬â„¢s was making in his book Ã¢â‚¬Å“The Edge of EvolutionÃ¢â‚¬Â. This was written in debate on another blog in response to a question on how parasites mutates to adapt to antibiotics/insecticides. This is what made me think of that question above.

1. The malaria parasite isn't limited by temperature, the mosquito that transmits it is what's limited by temperature, because standing water is most common in tropical areas with large amounts of rainfall. It'd be interesting to see how an internal parasite could evolve a way to control rainfall and evaporation . And just in case your wondering why malaria can't evolve a way to eliminate the dependancy on mosquitoes, human to human transmission of malaria is pretty much impossible (red blood cells don't get shared by humans very often unless its from an insect bite).

2. Sickle cell doesn't do anything directly to the malaria parasite. Malaria parasites live and reach maturity in red blood cells. A person with sickle cell has red blood cells that die and get replaced at a faster rate than normal (causing anemia). When the red blood cell dies, the parasite inside also dies. Because the red blood cells die faster the concentration of malaria parasites in sickle cell humans is usually low enough to avoid the major problems caused by malaria even though there are still some parasites present. Thinking malaria should evolve resistance to sickle cell is kind of like saying since tornadoes keep destroying houses and killing the humans inside, humans should have evolved a resistance to tornadoes.

The only way to "beat" sickle cell would be to breed faster which would might be a bad thing for malaria if it wound up killing the non-sickle cell humans faster (the majority of potential hosts don't have sickle cell and from a parasites perspective, killing a host faster is usually a bad thing).

Wiki on MalariaIn the merozoite stage of its life cycle the malaria parasite lives inside red blood cells, and its metabolism changes the internal chemistry of the red blood cell. Infected cells normally survive until the parasite reproduces, but if the red cell contains a mixture of sickle and normal haemoglobin, it is likely to become deformed and be destroyed before the daughter parasites emerge

First of all, a parasite that makes its host die out is a very unsuccessful parasite. Obviously, killing your host is rather a bad idea if you're a parasite.

A parasite is really a wannabe symbiotic partner. Most parasites fail symbiosis and must make do with allowing their host to survive, at least long enough to spread to a new host. Since the malaria parasite is dependent on two hosts, it is even more unlikely to benefit from being too virulent.

However, there is another point. Creationists often point out how unlikely some specific evolution step is. Then they turn around and ask, "so why didn't this or that evolution happen?"

Now, there are two reasonable answers to that:

- It just didn't happen to occur.

- The organism in question does not have the potential for that adaption. For an adaption to happen, the organism must not only have the luck to have the right mutation, it must also have some genetic material that can change to give the adaption.

1. The malaria parasite isn't limited by temperature, the mosquito that transmits it is what's limited by temperature, because standing water is most common in tropical areas with large amounts of rainfall. It'd be interesting to see how an internal parasite could evolve a way to control rainfall and evaporation . And just in case your wondering why malaria can't evolve a way to eliminate the dependancy on mosquitoes, human to human transmission of malaria is pretty much impossible (red blood cells don't get shared by humans very often unless its from an insect bite).

2. Sickle cell doesn't do anything directly to the malaria parasite. Malaria parasites live and reach maturity in red blood cells. A person with sickle cell has red blood cells that die and get replaced at a faster rate than normal (causing anemia). When the red blood cell dies, the parasite inside also dies. Because the red blood cells die faster the concentration of malaria parasites in sickle cell humans is usually low enough to avoid the major problems caused by malaria even though there are still some parasites present. Thinking malaria should evolve resistance to sickle cell is kind of like saying since tornadoes keep destroying houses and killing the humans inside, humans should have evolved a resistance to tornadoes.

The only way to "beat" sickle cell would be to breed faster which would might be a bad thing for malaria if it wound up killing the non-sickle cell humans faster (the majority of potential hosts don't have sickle cell and from a parasites perspective, killing a host faster is usually a bad thing).

Wiki on MalariaIn the merozoite stage of its life cycle the malaria parasite lives inside red blood cells, and its metabolism changes the internal chemistry of the red blood cell. Infected cells normally survive until the parasite reproduces, but if the red cell contains a mixture of sickle and normal haemoglobin, it is likely to become deformed and be destroyed before the daughter parasites emerge

This is from Behe's Book " The Edge of Evoultion" Please read:

Time is actually not the chief factor in evolution- population numbers are. In calculating how quickly a beneficial mutation might appear, evolutionary biologist multiplies the mutation rate by the population size. Since for many kinds of organisms the mutation rate is pretty similar, the waiting time for the appearance of the helpful mutations depends mostly on members of organisms: The bigger the population or the faster the reproduction cycle, the more quickly a particular mutation will show. The numbers of malaria cells and HIV in just the past fifty years have probably greatly surpassed the number of mammals that have lived on the earth in the past several hundred million years. So the evolutionary behavior of pathogens in even such a short time as a half a century gives us a clear indication what can happen with larger organism over enormous time spans. The fact that no new cellular protein-protein interactions were fashioned, that mutations were incoherent, That changes in only a few genes where able to help, and that those changes where only relatively(not absolutely) beneficial- at that gives us a strong reason to expect the same for larger organisms over longer times.

In other words, malaria in just the last 50 years could easily have larger numbers than all the mammal life put together in the history of the earth. Mammals have undergone tremendous macro-evolution on every species. Why, donÃ¢â‚¬â„¢t we see even small macro-evolutionary changes with malaria? We have seen micro-evolutionary changes. The numbers are there.

]2. Sickle cell doesn't do anything directly to the malaria parasite. Malaria parasites live and reach maturity in red blood cells. A person with sickle cell has red blood cells that die and get replaced at a faster rate than normal (causing anemia). When the red blood cell dies, the parasite inside also dies. Because the red blood cells die faster the concentration of malaria parasites in sickle cell humans is usually low enough to avoid the major problems caused by malaria even though there are still some parasites present. Thinking malaria should evolve resistance to sickle cell is kind of like saying since tornadoes keep destroying houses and killing the humans inside, humans should have evolved a resistance to tornadoes.

Sickle cell is advantageous when there the person has only one sickle cell gene from a patent. When two genes are present then the person is very sick or dies. The people with only one gene usually have few or no heath problems. In other words, the hemoglobin will not solidify on its own-it needs a further push: Malaria provides that push. Therefore, malaria could conceivably beat sickle cell by providing a stabilizer: Just one example of many.

1. The malaria parasite isn't limited by temperature, the mosquito that transmits it is what's limited by temperature, because standing water is most common in tropical areas with large amounts of rainfall. It'd be interesting to see how an internal parasite could evolve a way to control rainfall and evaporation . And just in case your wondering why malaria can't evolve a way to eliminate the dependancy on mosquitoes, human to human transmission of malaria is pretty much impossible (red blood cells don't get shared by humans very often unless its from an insect bite).

Malaria most commonly is found in warmer regions of the world that have tropical and subtropical climates. Anopheles mosquitoes thrives in higher temperatures, and malaria parasites, which grow and develop inside mosquitoes, need warmth in order to grow to a maturity stage in which they can be transmitted to humans.

There are two factors here: (1) need warmth in order to grow to a maturity stage and 2) Anopheles mosquitoes which is a warm weather mosquitoes. Why hasnÃ¢â‚¬â„¢t malaria evolved and grow to maturity in cold weather? Why hasnÃ¢â‚¬â„¢t it evolved to colder weather mosquitoes?

The only way to "beat" sickle cell would be to breed faster which would might be a bad thing for malaria if it wound up killing the non-sickle cell humans faster (the majority of potential hosts don't have sickle cell and from a parasites perspective, killing a host faster is usually a bad thing).

This assumes that random mutation or malaria thinks or has intelligence. Taking it from a parasites perspective is nonsense- it does not anticipate consequences-that requires intelligence.

url=http://en.wikipedia.org/wiki/Malaria]Wiki on Malaria[/url]In the merozoite stage of its life cycle the malaria parasite lives inside red blood cells, and its metabolism changes the internal chemistry of the red blood cell. Infected cells normally survive until the parasite reproduces, but if the red cell contains a mixture of sickle and normal hemoglobin, it is likely to become deformed and be destroyed before the daughter parasites emerge

The sickle cell hemoglobin acts like magnets and they gel or coagulate. The mechanism that beats sickle cell isn't a fragile cell but the hemoglobin plating.

This is from Behe's Book " The Edge of Evoultion" Please read:In other words, malaria in just the last 50 years could easily have larger numbers than all the mammal life put together in the history of the earth. Mammals have undergone tremendous macro-evolution on every species. Why, donÃ¢â‚¬â„¢t we see even small macro-evolutionary changes with malaria? We have seen micro-evolutionary changes. The numbers are there.

Generally large scale changes in a population require significant selective pressure. Anti-malarial drugs could be considered the biggest selective pressure faced by malaria in modern times and there have certainly been mutations making malaria resistant to these drugs. I don't know about specific protein-protein interactions in malaria but I do know that Behe has acknowledged that new protein-protein interactions have been seen to evolve in HIV (along with the expected argument that it doesn't really count).

LinkYes, IÃ¢â‚¬â„¢m perfectly willing to concede that this does appear to be the development of a new viral protein-viral protein binding site, one which I overlooked when writing about HIV......This situation is probably best viewed as a foreign protein degrading the integrity of a membrane, rather than performing some positive function.

Sickle cell is advantageous when there the person has only one sickle cell gene from a patent. When two genes are present then the person is very sick or dies. The people with only one gene usually have few or no heath problems. In other words, the hemoglobin will not solidify on its own-it needs a further push: Malaria provides that push. Therefore, malaria could conceivably beat sickle cell by providing a stabilizer: Just one example of many.

1. Is such a stabilizer possible? If so why can't sickle cell be treated with this stabilizer?2. What effect would such a stabilizer have on normal phenotype humans? If it kills them it's a net loss for malaria.3. Given that heterozygous sickle cell humans make up a significantly smaller percentage of the population than normal phenotype humans, and given that malaria parasites still survive in heterozygous individuals, just at lower concentrations, how large is the selective pressure on malaria to evolve a response?

There are two factors here: (1) need warmth in order to grow to a maturity stage and

1. At what point in the malarial life stage is it directly exposed to the outside temp? As far as I know it goes from mosquito->human->mosquito without encountering the outside enviroment.2. Mosquitoes are most common in warm weather areas since all mosquitoes use pools of water to lay eggs. It's also entirely consistent with evolution for something to become specialized to a specific ecological niche, such as living in a particular species of mosquito. There's no reason to expect that such a specialization would be reversed.

This assumes that random mutation or malaria thinks or has intelligence. Taking it from a parasites perspective is nonsense- it does not anticipate consequences-that requires intelligence.The sickle cell hemoglobin acts like magnets and they gel or coagulate. The mechanism that beats sickle cell isn't a fragile cell but the hemoglobin plating.

I wasn't suggesting that malaria has intelligence. I was suggesting something similar to MRC_Hans when he said "First of all, a parasite that makes its host die out is a very unsuccessful parasite. Obviously, killing your host is rather a bad idea if you're a parasite."

A parasite that kills it's host before it can spread is a parasite that doesn't spread it's genes. Basically, the more virulant a disease, the less likely it is to succeed. Malaria hasn't wiped out humans because any variations of malaria that kill off humans quickly ends up dieing when the human host dies. A malaria variation that kills humans slowly enough that the human population can remain stable will be the only variations that will continue to exist.

Generally large scale changes in a population require significant selective pressure. Anti-malarial drugs could be considered the biggest selective pressure faced by malaria in modern times and there have certainly been mutations making malaria resistant to these drugs. I don't know about specific protein-protein interactions in malaria but I do know that Behe has acknowledged that new protein-protein interactions have been seen to evolve in HIV (along with the expected argument that it doesn't really count)

LinkYes, IÃ¢â‚¬â„¢m perfectly willing to concede that this does appear to be the development of a new viral protein-viral protein binding site, one which I overlooked when writing about HIV......This situation is probably best viewed as a foreign protein degrading the integrity of a membrane, rather than performing some positive function.

Behe was saying that having two protein-protein beneficial mutations was beyond evolutions power. This is just one, so it still fits his thesis.

1. Is such a stabilizer possible? If so why can't sickle cell be treated with this stabilizer?2. What effect would such a stabilizer have on normal phenotype humans? If it kills them it's a net loss for malaria.

The stabilizer was a hypothetical for malaria overcoming sickle cell: Life has been very ingenious on how it has surmounted obstacles. My hypothetical was not intended to state how malaria would overcome sickle cell, rather that it could.

3. Given that heterozygous sickle cell humans make up a significantly smaller percentage of the population than normal phenotype humans, and given that malaria parasites still survive in heterozygous individuals, just at lower concentrations, how large is the selective pressure on malaria to evolve a response?1. At what point in the malarial life stage is it directly exposed to the outside temp? As far as I know it goes from mosquito->human->mosquito without encountering the outside enviroment.2. Mosquitoes are most common in warm weather areas since all mosquitoes use pools of water to lay eggs. It's also entirely consistent with evolution for something to become specialized to a specific ecological niche, such as living in a particular species of mosquito. There's no reason to expect that such a specialization would be reversed.

It is also consistent for life to move beyond its ecological niche- The diversity of life every where suggest that it has.

Has there been any research quantifying selective pressure? What interested me most about your answer is that your told me why evolution could not, or would not, overcome these barriers: In other words why malaria hasnÃ¢â‚¬â„¢t evolved recently. Yet I can say that if macro-evolution where true then we would have overcome far bigger hurtles, built intricate systems with far less selective pressure and fewer numbers. For example,

Although we retain some minor veto power (like holding our breath, taking a laxative, or postponing a meal), the vast majority of our physiological functions are self-regulating system, your body constantly monitors your oxygen concentration, carbon dioxide levels, blood pressure, heart rate, kidney functions, immune stats, balance, salt concentrations, internal temperature and controls, hydration status and corrective actions, red and white blood cell productions, saliva production, gastric juice production, bowel movements, bile production, fatigue levels, a myriad of hormone levels and their impact, tactile signals and your responses, blood sugar and insulin levies, and sounds, sight, and smells. Should your oxygen levels drop below a safe concentration or your carbon dioxide concentrations rise too high, you will automatically breathe faster, deeper, or both. If you walk fast or climb stairs, your heart rate increases in appropriate increments. Imagine some ancient, intermediate species that kept passing out because its hear or lungs couldntÃ¢â‚¬â„¢t keep up. Or one who had to concentrate on where his might be for every chew to avoid constant lacerations.Merely every living being has an incredible capability to monitory and repair itselfÃ¢â‚¬Â¦

From Billions of Missing Links by Geoffrey Simmons M.D. Page 138. I typed it- so there my be errors.

I wasn't suggesting that malaria has intelligence. I was suggesting something similar to MRC_Hans when he said "First of all, a parasite that makes its host die out is a very unsuccessful parasite. Obviously, killing your host is rather a bad idea if you're a parasite."

A parasite that kills it's host before it can spread is a parasite that doesn't spread it's genes. Basically, the more virulant a disease, the less likely it is to succeed. Malaria hasn't wiped out humans because any variations of malaria that kill off humans quickly ends up dieing when the human host dies. A malaria variation that kills humans slowly enough that the human population can remain stable will be the only variations that will continue to exist.

Yep, I made a mistake: I answered my question rather than yours. My question was why hasnÃ¢â‚¬â„¢t evolution created a strain that is unbeatable by man? Yes, if that strain kills the host too quickly it will die off.

The question is still, why have we only seen micro, not macro, evolutionary changes to malaria when the numbers of malaria are so large: worldwide in one year are ~10^20? With these huge numbers we should see selective pressure and evolution do a great deal more: Especially considering the intricate well balanced systems evolution has supposedly developed (see quote above) with far fewer numbers.

The question is still, why have we only seen micro, not macro, evolutionary changes to malaria when the numbers of malaria are so large: worldwide in one year are ~10^20? With these huge numbers we should see selective pressure and evolution do a great deal more: Especially considering the intricate well balanced systems evolution has supposedly developed (see quote above) with far fewer numbers.

I'm sorry, but you are committing a fallacy that we often see ("we" meaning people who engage into debates like this). First you admit to knowing very little about evolution. No problem in this, you are a honest seeker. But then you imagine how you think things ought to happen and demand that we explain why it doesn't.

The basic answer to your question is that if you study evolution thoroughly enough, you will realize that your assumption about how malria should evolve is not valid, it is built on your present lack of knowledge.

I know you are not doing this deliberately (I have sometimes met people that do), but the answer to this question lies in long lectures on evolution mechanisms, there is no precise short answer.

Ask all you want, and don't fear making stupid questions, because they don't exist, but try to avoid making assumptions.

I'm sorry, but you are committing a fallacy that we often see ("we" meaning people who engage into debates like this). First you admit to knowing very little about evolution. No problem in this, you are a honest seeker. But then you imagine how you think things ought to happen and demand that we explain why it doesn't.

The basic answer to your question is that if you study evolution thoroughly enough, you will realize that I know you are not doing this deliberately (I have sometimes met people that do), but the answer to this question lies in long lectures on evolution mechanisms, there is no precise short answer.

Ask all you want, and don't fear making stupid questions, because they don't exist, but try to avoid making assumptions.

Hans

Hans

Hans,

I don't know much about fossils, which is not a lack of understanding of evolution: Evolution is a big subject. I here statements like " your assumption about how malria should evolve is not valid, it is built on your present lack of knowledge." all the time. There is an arrogance to that answer; It presumes that you have the answers while never having to answer the question. I have seen evolutionist do this elitist "I know better answer" exclusively in other blogs.

Admitting that you don't know something is honest, if you are honest you can get to the truth. Presuming you have the answer and fitting all the facts to the preordained answer is not honest: Excluding alternatives is not honest. Evolutionist has not been proven and shutting off the debate is unscientific.

Hans, this rant really isn't directed at you. I am very frustrated on how evolution is debated.

I don't know much about fossils, which is not a lack of understanding of evolution: Evolution is a big subject. I here statements like " your assumption about how malria should evolve is not valid, it is built on your present lack of knowledge." all the time. There is an arrogance to that answer; It presumes that you have the answers while never having to answer the question. I have seen evolutionist do this elitist "I know better answer" exclusively in other blogs.

Admitting that you don't know something is honest, if you are honest you can get to the truth. Presuming you have the answer and fitting all the facts to the preordained answer is not honest: Excluding alternatives is not honest. Evolutionist has not been proven and shutting off the debate is unscientific.

Hans, this rant really isn't directed at you. I am very frustrated on how evolution is debated.

That was not what I meant. The problem is that people make assumptions and then ask for an explanation why the assumption is wrong. But on any complex matter, and evolution is certainly very complex, you can always pick out some detail that, when viewed in isolation, looks counterintuitive. You can then say, "hey, I feel this should have been so and so, kindly explain why not". And the other side can go on forever trying to dismember assumptions that are really based on insuffucuent knowledge or context.

For example malaria. You ask why malaria hasn't won the arms race against humanity, but you could ask that about any species. Why haven't lions won the race against zebras so they can catch them easily? Why haven't zebras won the arms race against lions, so they can always get away? The short answer is that they just haven't. If malaria had won out over humans, neither of us (humans and malaria) would be around any longer.

That was not what I meant. The problem is that people make assumptions and then ask for an explanation why the assumption is wrong. But on any complex matter, and evolution is certainly very complex, you can always pick out some detail that, when viewed in isolation, looks counterintuitive. You can then say, "hey, I feel this should have been so and so, kindly explain why not". And the other side can go on forever trying to dismember assumptions that are really based on insuffucuent knowledge or context.

For example malaria. You ask why malaria hasn't won the arms race against humanity, but you could ask that about any species. Why haven't lions won the race against zebras so they can catch them easily? Why haven't zebras won the arms race against lions, so they can always get away? The short answer is that they just haven't. If malaria had won out over humans, neither of us (humans and malaria) would be around any longer.

Hans

Hi Hans,

The reason I chose malaria was because it has such a large sample size. When each host has 1 trillion parasites and that there are 500-700 million hosts/year then you have a substantial sample size. With large sample sizes you can quantify the how often mutations occur -specifically beneficial (loosely defined) mutations. You can also say how often that you can have multiple mutations, specifically 2, that can have a beneficial benefit.

The point really really about why hasn't malaria won out, my real point is why haven't we seen macro-evolution in real living organisms.

In fact I don't care if you use malaria, HIV (which mutates 10,000 time faster), Dr. Lenski's e-coli, bacteria or say insects: We have huge sample sizes and we should see macro-evolution. We don't. We see 1-2 beneficial mutations but as far as I know never more. We don't see systems being built or anything close to macro-evolution: Why haven't we?

The reason I chose malaria was because it has such a large sample size. When each host has 1 trillion parasites and that there are 500-700 million hosts/year then you have a substantial sample size. With large sample sizes you can quantify the how often mutations occur -specifically beneficial (loosely defined) mutations. You can also say how often that you can have multiple mutations, specifically 2, that can have a beneficial benefit.

The point really really about why hasn't malaria won out, my real point is why haven't we seen macro-evolution in real living organisms.

In fact I don't care if you use malaria, HIV (which mutates 10,000 time faster), Dr. Lenski's e-coli, bacteria or say insects: We have huge sample sizes and we should see macro-evolution. We don't. We see 1-2 beneficial mutations but as far as I know never more. We don't see systems being built or anything close to macro-evolution: Why haven't we?

Bruce

Hi Bruce,
There at least 200 species of the Plasmodium parasite out there. Most of these have become specialized to particular animals. There are 70 species species of avian malaria alone. Geneticists (including my wife) are currently tracking the evolutionary changes and evolutionary history of the plasmodium parasite. Here is a link from the Proceedings of the National Academy.

I would say that the Plasmodium has won in many parts of the world. Winning in evolutionary terms means "successfully reproducing", not killing your host. The plasmodium has successfully adapted to a wide range of animals. In upstate NY, about 10% to 15% of the bird population has the avian bird malaria (so my wife tells me) - and they are trying to figure out why this malaria is not currently transmitted to people. And yes, it continues to evolve as noted in the link above.

Hi Bruce,
There at least 200 species of the Plasmodium parasite out there. Most of these have become specialized to particular animals. There are 70 species species of avian malaria alone. Geneticists (including my wife) are currently tracking the evolutionary changes and evolutionary history of the plasmodium parasite. Here is a link from the Proceedings of the National Academy.

I would say that the Plasmodium has won in many parts of the world. Winning in evolutionary terms means "successfully reproducing", not killing your host. The plasmodium has successfully adapted to a wide range of animals. In upstate NY, about 10% to 15% of the bird population has the avian bird malaria (so my wife tells me) - and they are trying to figure out why this malaria is not currently transmitted to people. And yes, it continues to evolve as noted in the link above.

Hope that helps.
James

Hi James,

Good posting as always.

I can't get the article you posted to come up.

I have some questions:

1. Are these strains new? Have we seen this evolution within the last 50 years with these examples?
2. When was the article written?

This looks like the holy grail of evolution. Absolute proof in real time. This is or should be big news. I will look into this further. May be a few days.

Behe's entire book "the edge of evolution" was on how we have not seen 3+ mutations or 3+ new protein-protein interactions. His specialty is or was malaria and he multiple examples. If what you have posted is proof of multiple positive mutations that would disprove his book. Behe is answering questions like this on his amazon web site.

1. Are these strains new? Have we seen this evolution within the last 50 years with these examples?2. When was the article written?

This looks like the holy grail of evolution. Absolute proof in real time. This is or should be big news. I will look into this further. May be a few days.

God Bless,Bruce

Hi Bruce,

The picture I showed in that post was for larger species changes. There are a number of subspecies changes within the species Plasmodium Falciparum (the one that infects humans). I don't know what counts as the holy grail. These kinds of things are found all the time if you just look a bit. For example, in Malawi where the plasmodium became drug resistant, they found that the plasmodium had developed / evolved four mutations.

http://lib.bioinfo.pl/pmid:12659974High prevalence of quintuple mutant dhps/dhfr genes in Plasmodium falciparum infections seven years after introduction of sulfadoxine and pyrimethamine as first line treatment in Malawi.

Behe's entire book "the edge of evolution" was on how we have not seen 3+ mutations or 3+ new protein-protein interactions. His specialty is or was malaria and he multiple examples. If what you have posted is proof of multiple positive mutations that would disprove his book. Behe is answering questions like this on his amazon web site.

If you saw the the Intelligent Design show on NOVA, you will probably note that academics don't take Behe very seriously. To his credit, he makes statements that can be tested. However, for most of the academic community, they have been tested and he has been proven wrong. I doubt you could even get a paper published proving him wrong, because it would be like proving the earth really does go around the sun.

In my opinion, Behe's main misunderstanding of evolutionary theory is his failure to recognize the sequence of mutations that might lead to a particular trait. If you want to read a bit of evolutionary biology on the issue, you might try the article by Stephen J. Gould Leowentin here on page 73.

The basic idea is the following: Suppose mutation A is somewhat useful for a problem #1 (e.g., makes you swim faster, more resistant to the ) so it spreads through the gene pool.

Mutation B in addition to A is even more useful (although B on its own is useless).

Ok now the interesting step. Suppose new Mutation C with mutation B is magnificent. Imagine it is so good that the gene with Mutation A is not even required any more. And suppose C is not useful without B.

Each of these steps can be microevolutionary steps. However, if you looked at the finished system you might say this is irreducibly complex because B mutation on its own is useless and mutation C on its own is useless, and the probability of the two together is much too rare. The problem is that with the finished product you may not know that mutation A played a big role.

This may seem a bit odd, but it is argued by many evolutionary theorists that such a progression is quite common. I can give a few examples if you like.

Hope that helps, James

p.s. if you are ever curious as to who is an expert in academia, or want to know what people think of some work, you can go Google Scholar and see who cites the work. For example, here is Michael Behe's academic work.

*snip*We have huge sample sizes and we should see macro-evolution. We don't. We see 1-2 beneficial mutations but as far as I know never more.

*snip*

My bolding. Why should we see that? In my country we have 300+ traffic deaths a year (we are only 5 million people), and I have been driving for over 40 years. I should have seen somebody killed. I haven't (thank God). Why not?

.... This just to demonstrate that such questions don't really make sense.

This looks like the holy grail of evolution. Absolute proof in real time. This is or should be big news.

I'm really sorry, Bruce, but no. It's not big news. Not to evolutionists. I realize that the mantra about evolution being just a desparate illusion with no real backing has been repeated so often in creationist circles, that you have probably come to believe it, but out here, it's old news. We have not been waiting anxiously for the final vindication. That came long ago.

The picture I showed in that post was for larger species changes. There are a number of subspecies changes within the species Plasmodium Falciparum (the one that infects humans). I don't know what counts as the holy grail. These kinds of things are found all the time if you just look a bit. For example, in Malawi where the plasmodium became drug resistant, they found that the plasmodium had developed / evolved four mutations.

http://lib.bioinfo.pl/pmid:12659974High prevalence of quintuple mutant dhps/dhfr genes in Plasmodium falciparum infections seven years after introduction of sulfadoxine and pyrimethamine as first line treatment in Malawi.If you saw the the Intelligent Design show on NOVA, you will probably note that academics don't take Behe very seriously. To his credit, he makes statements that can be tested. However, for most of the academic community, they have been tested and he has been proven wrong. I doubt you could even get a paper published proving him wrong, because it would be like proving the earth really does go around the sun.

In my opinion, Behe's main misunderstanding of evolutionary theory is his failure to recognize the sequence of mutations that might lead to a particular trait. If you want to read a bit of evolutionary biology on the issue, you might try the article by Stephen J. Gould Leowentin here on page 73.

The basic idea is the following: Suppose mutation A is somewhat useful for a problem #1 (e.g., makes you swim faster, more resistant to the ) so it spreads through the gene pool.

Mutation B in addition to A is even more useful (although B on its own is useless).

Ok now the interesting step. Suppose new Mutation C with mutation B is magnificent. Imagine it is so good that the gene with Mutation A is not even required any more. And suppose C is not useful without B.

Each of these steps can be microevolutionary steps. However, if you looked at the finished system you might say this is irreducibly complex because B mutation on its own is useless and mutation C on its own is useless, and the probability of the two together is much too rare. The problem is that with the finished product you may not know that mutation A played a big role.

This may seem a bit odd, but it is argued by many evolutionary theorists that such a progression is quite common. I can give a few examples if you like.

Hope that helps, Jamesp.s. if you are ever curious as to who is an expert in academia, or want to know what people think of some work, you can go Google Scholar and see who cites the work. For example, here is Michael Behe's academic work.

As you will see, there are no entries. From this, I would not conclude he was an expert on malaria, but he has done some reputable work.

Hi James,

I feel the Nova show was propaganda and looked more like a Micheal Moore movie than serious science. I have seen Dr. Behe slammed in very personal ways by the intelligentsia. This frustrates me because personal attacks and propaganda are the tools of politics and IMO has no home in science. Science is becoming more and more political and less and less scientific: global warming, stem cell ...

Dr. Ken Miller was trying to discredit Irreducible complexity and Dr. Behe: he did neither The debate showed that evolutionist has no idea how flagellum has evolved.(This is the flagship paper to discredit Behe)

See figure I in Millers paper for a picture and description of flagellum.

An irreducibly complex (IC) structure is defined as ". . . a single system composed of several well-matched, interacting parts that contribute to the basic function, wherein the removal of any one of the parts causes the system to effectively cease functioning." (Behe)

This is Dr. Ken Miller argument in a nutshell:

Invading bacteria introduced one building block of flagellum into a cell by DNA or protein transfer. (See Figure II). This proves two things: (1) the flagellum could be built in large units using readily available building blocks and (2) the TTSS (see quote 2 below) is a functional system independent of the flagellum. So flagellum did not need to be made piece meal and its parts could survive outside the IC system.

Summary in Millers words:

The contention that the flagellum must be fully-assembled before any of its component parts can be useful is obviously incorrect. What this means is that the argument for intelligent design of the flagellum has failed.Ã¢â‚¬Â

Now that a simpler, functional system (the TTSS) has been discovered among the protein components of the flagellum, the claim of irreducible complexity has collapsed, and with it any "evidence" that the flagellum was designed.

quote 2- what TTSS is from Miller

In order to carry out this diabolical work, bacteria must not only produce the protein toxins that bring about the demise of their hosts, but they must efficiently inject them across the cell membranes and into the cells of their hosts. They do this by means of any number of specialized protein secretory systems. One, known as the type III secretory system (TTSS), allows gram negative bacteria to translocate proteins directly into the cytoplasm of a host cell (Heuck 1998)

Problems with Millers paper: (I got most of the arguments from William Dembski paper) (I cut and pasted liberally)

Design theorists, in attributing design to systems that exhibit IC, are simply doing what scientists do generally, which is to attempt to formulate a causally adequate explanation of the phenomenon in question. Using flagellum as an example of IC is similar as Darwin using finchÃ¢â‚¬â„¢s to describe evolution.

1. However, taking away the parts of the flagellum certainly destroys the ability of the system to act as a rotary propulsion machine. Thus, contra Miller, the flagellum is indeed irreducibly complex.

2. The best current molecular evidence, however, points to the TTSS as evolving from the flagellum and not vice versa (Nguyen et al. 2000). In other words: The first building block to flagellum was not available as a building block for the first flagellum. It follows that the TTSS does not explain the evolution of the flagellum

The whole point of bringing up the TTSS was to posit it as an evolutionary precursor to the bacterial flagellum. The best current molecular evidence, however, points to the TTSS as evolving from the flagellum and not vice versa (Nguyen et al. 2000). This can also be seen intuitively. The bacterial flagellum is a motility structure for propelling a bacterium through its watery environment. Water has been around since the origin of life. But the TTSS, as Mike Gene (see citation at end) notes, is restricted "to animal and plant pathogens." Accordingly, the TTSS could only have been around since the rise of metazoans. Gene continues: "In fact, the function of the system depends on intimate contact with these multicellular organisms. This all indicates this system arose after plants and animals appeared. In fact, the type III genes of plant pathogens are more similar to their own flagellar genes than the type III genes of animal pathogens. This has led some to propose that the type III system arose in plant pathogens and then spread to animal pathogens by horizontal transfer.... When we look at the type III system its genes are commonly clustered and found on large virulence plasmids. When they are in the chromosome, their GC content is typically lower than the GC content of the surrounding genome. In other words, there is good reason to invoke horizontal transfer to explain type III distribution. In contrast, flagellar genes are usually split into three or more operons, they are not found on plasmids, and their GC content is the same as the surrounding genome. There is no evidence that the flagellum has been spread about by horizontal transfer."

3. The TTSS is after all much simpler than the flagellum. The TTSS contains ten or so proteins that are homologous to proteins in the flagellum. The flagellum requires an additional thirty or forty proteins, which are unique. Evolution needs to explain the emergence of complexity from simplicity. But if the TTSS evolved from the flagellum, then all we've done is explain the simpler in terms of the more complex. (my add- TTSS accounts for 1/4 or flagellum, Miller made no attempt to account for the the 3/4 of the proteins that make flagellum)

4. All of this is highly speculative, and accounts for cell biologist Franklin Harold's (2001, 205) frank admission: "There are presently no detailed Darwinian accounts of the evolution of any biochemical or cellular system, only a variety of wishful speculations." (Miller knows and respects Franklin Harold's: He is not an I.D.er.)

This is only up to page 4/13 from Dembski article.

My summary,

Dr. Miller did not disprove Intelligent Design, irreducibly complexity or that flagellum was not irreducibly complex. The strongest arguement IMO was -"The best current molecular evidence, however, points to the TTSS as evolving from the flagellum and not vice versa." Dr. Dembski disproved Millers FFSS hypothetical and showed that evolutionist has no idea how flagellum evolved: zero idea.

What makes me mad is that Millers paper is the flagship paper which supposedly disproves I.D. and discredits Behe.

Hi Bruce,
There at least 200 species of the Plasmodium parasite out there. Most of these have become specialized to particular animals. There are 70 species species of avian malaria alone. Geneticists (including my wife) are currently tracking the evolutionary changes and evolutionary history of the plasmodium parasite. Here is a link from the Proceedings of the National Academy.

I would say that the Plasmodium has won in many parts of the world. Winning in evolutionary terms means "successfully reproducing", not killing your host. The plasmodium has successfully adapted to a wide range of animals. In upstate NY, about 10% to 15% of the bird population has the avian bird malaria (so my wife tells me) - and they are trying to figure out why this malaria is not currently transmitted to people. And yes, it continues to evolve as noted in the link above.

Hope that helps.
James

When I see a tree like this I donÃ¢â‚¬â„¢t know really what it says and it raises more question than it answers. For example,

1. Are any of these different strains caused by mendelian variation. Somewhat like dogs, we can get a great diversity within the current genome. Hence, Mendelian variations tell us nothing about how the genetic information in the present stock arose and it is not the sort of change required to demonstrate Ã¢â‚¬ËœupwardÃ¢â‚¬â„¢ evolutionÃ¢â‚¬â€there has been no addition of new and useful Ã¢â‚¬ËœsentencesÃ¢â‚¬â„¢.
2. The article says that many of these variations where caused my mutation. But it doesnÃ¢â‚¬â„¢t say if the mutations where beneficial or exactly what made one variation different than the others. Generally, mutations decrease order, and since all of our observations and our understanding of entropy tells us that in a natural, spontaneous, unguided and unprogrammed process order will decrease, the same will be true of information within the genome. Therefore, unless show otherwise, I have to assume these mutated varieties of malaria do not show an upward evolutionary progression.

I also pulled this from the article:

P. falciparum is more closely related to Plasmodium reichenowi, the chimpanzee parasite, than to any other Plasmodium species. The time of divergence between these two Plasmodium species is estimated at 8-12 million years ago, which is roughly consistent with the time of divergence between the two host species, human and chimpanzee.

This states in my words, that chimpanzees evolved into man during this 8-12 million year interval. This is a radical change with very few numbers relatively speaking. On the other hand, we see Plasmodium reichenowi evolving into P. falciparum during that time: This is an extremely small change considering that huge numerical advantage that it has on the host. From my understanding of evolution I would think the reverse would be true: That malaria with its large numbers would have evolved for more than the chimpanzee. Why is that?

The picture I showed in that post was for larger species changes. There are a number of subspecies changes within the species Plasmodium Falciparum (the one that infects humans). I don't know what counts as the holy grail. These kinds of things are found all the time if you just look a bit. For example, in Malawi where the plasmodium became drug resistant, they found that the plasmodium had developed / evolved four mutations.

http://lib.bioinfo.pl/pmid:12659974High prevalence of quintuple mutant dhps/dhfr genes in Plasmodium falciparum infections seven years after introduction of sulfadoxine and pyrimethamine as first line treatment in Malawi.

Hi James,

In truth I read this article and I didn't really understand it. Here is a quote:

Two isolates contained the dhps single or double mutant coupled with dhfr wild-type. The high prevalence rates of the three dhfr mutations in our study were consistent with a previous survey in 1995 in Karonga, Malawi, whereas the prevalences of dhps mutations had increased, most probably as a result of the wide use of SP. A total of 52 P. falciparum isolates were also investigated for pyrimethamine and sulfadoxine/pyrimethamine activity against parasite growth according to WHO in vitro standard protocol. A pyrimethamine resistant profile was found. When pyrimethamine was combined with sulfadoxine, the mean EC(50) value decreased to less than one tenth of the pyrimethamine alone level. This synergistic activity may be explained by sulfadoxine inhibition of dhps despite the double mutations in the dhps genes, which would interact with pyrimethamine acting to block the remaining folate despite dhfr mutations in the low p-aminobenzoic acid and low folic acid medium mixed with blood.

I underlined what looks to be the mechanism of the 4 mutation. That is a double mutation combining with another wild strain.

My understanding of the thesis of Behe's book was that more than 2 beneficial mutations within a strain was beyond evolution. I do not know if these where beneficial mutations or exactly what they are: I just know the number was four. Consequently, I do not if new information was generated. Was this strain was an evolutionary improvement?

In truth I read this article and I didn't really understand it. Here is a quote:I underlined what looks to be the mechanism of the 4 mutation. That is a double mutation combining with another wild strain.

My understanding of the thesis of Behe's book was that more than 2 beneficial mutations within a strain was beyond evolution. I do not know if these where beneficial mutations or exactly what they are: I just know the number was four. Consequently, I do not if new information was generated. Was this strain was an evolutionary improvement?

Hi Bruce,First, I can't say I understand Behe's point so it is hard to criticize directly. However, I can say that if one were to look at animal breeds developed by artificial selection, I am fairly sure we can find lots of cases where the breeds differ by multiple mutations. However, it is always difficult to determine what mutations produce particular traits - so it is difficult to say something like "the new breed showed 4 mutations and 3 of those are beneficial".

Suppose you were a pigeon breeder trying to get some interesting breed of fancy pigeon and after 200 generations you get this from a regular pigeon

Ok, now suppose you find that the new pigeon has 3 mutations in their genome. Were these beneficial? Did you need all three of the mutations to get this bird? You could try to do an experiment and change some of the genes back but that would take some clever gene splicing (but possible).

It is possible to also get these 3 different mutations sequentially, which some might consider to be a set of unsurprising micro-evolutionary steps.

I think Behe might be trying to argue that all three are unlikely to occur at the same time. But even there I would need to know the particular assumptions made. Suppose, for example, every new generation has 3 mutations on average at random places. Out of all the offspring with 3 mutations, I take the one I think looks pretty and allow those to breed. Ok, since at least one of those worked out, the answer is about 100% probability that the new breed will have 3 mutations.

None of this seems surprising to me. So I don't know what Behe finds surprising. I don't think he is arguing that plasmodia can't evolve resistance because we know it does. Is he suggesting that plasomodia is helped by God?

Behe appears to know the way most biologists believe 'information' gets added to the genome. To quote Behe:

"Gene duplication is thought to be a major source of evolutionary innovation because it allows one copy of a gene to mutate and explore genetic space while the other copy continues to fulfill the original function."

So he seems to know how it works, but he doesn't think it is probable enough. Unfortunately, I don't get his math.

James

p.s. The Nova show used transcripts to show what Behe and other said in the trial so I am not sure if you suggesting the show was unfair or that the judge in the trial was unfair.